Min-Hyun Kim

The Kim Laboratory investigates the molecular and epigenetic mechanisms that regulate energy homeostasis and contribute to the development of obesity and type 2 diabetes. Using rodent models and cell culture systems, our research focuses on understanding how nutritional factors influence hypothalamic signaling pathways that control appetite, energy expenditure, and glucose metabolism. By uncovering these mechanisms, we aim to develop innovative nutritional and therapeutic strategies to prevent and treat metabolic diseases.  

1. Epigenetic Regulation of Metabolic Hormone Signaling 

• Supported by the NIH/NIDDK (R01 DK139038) - Link to NIH RePORTER

Our research program investigates how epigenetic mechanisms regulate hypothalamic signaling pathways that control energy balance. We study how histone modifications, chromatin remodeling, DNA methylation, and microRNAs influence the expression and signaling of metabolic hormones, including leptin, GLP-1 and insulin, as well as their receptors. Our current NIH-funded project focuses on JMJD3, a histone demethylase that regulates hypothalamic leptin receptor expression and leptin sensitivity. 

2. Maternal Nutrition and Developmental Programming of Metabolic Health 

Early-life nutrition has lasting effects on metabolic health. We investigate how maternal obesity, undernutrition, and dietary composition influence hypothalamic development and metabolic hormone signaling in offspring. Our research aims to uncover the hormonal and epigenetic mechanisms that program lifelong susceptibility to obesity and metabolic disorders, with the goal of identifying strategies to improve metabolic health across generations. 

3. Nutritional Interventions to Improve Metabolic Health

We investigate how dietary interventions, including time-restricted feeding, calorie restriction, and dietary bioactive compounds, improve metabolic health by enhancing hypothalamic hormone signaling. Our research seeks to define the moleceular mechanisms underlying these nutritional interventions and evalute their potential to complement exisiting obesity therapies, including GLP-1-based therapies.